Abstract
The effects of boldine [(S)-2,9-dihydroxy-1,10-dimethoxyaporphine], a major alkaloid in the leaves and bark of boldo (Peumus boldus Mol.), on skeletal muscle were studied using mouse diaphragm and isolated sarcoplasmic reticulum membrane vesicles. Boldine, at 10-200 μM, has little effect on the muscle-evoked twitches; however, the ryanodine-induced contracture was potentiated dose-dependently. At higher concentrations of 300 μM, boldine by itself induced muscle contracture of two phases, which were caused by the influx of extracellular Ca2+ and induction of Ca2+ release from the internal Ca2+ storage site, the sarcoplasmic reticulum, respectively When tested with isolated sarcoplasmic reticulum membrane vesicles,boldine dose-dependently induced Ca2+ release from actively loaded sarcoplasmic reticulum vesicles isolated from skeletal muscle of rabbit or rat which was inhibited by ruthenium red, suggesting that the release was through the Ca2+ release channel, also known as the ryanodine receptor. Boldine also dose-dependently increased apparent [3H]-ryanodine binding with the EC50 value of 50 μM. In conclusion, we have shown that boldine could sensitize the ryanodine receptor and induce Ca2+ release from the internal Ca2+ storage site of skeletal muscle.
Original language | English |
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Pages (from-to) | 18-21 |
Number of pages | 4 |
Journal | Planta Medica |
Volume | 64 |
Issue number | 1 |
DOIs | |
Publication status | Published - 1998 |
Keywords
- Boldine
- Ca release
- Monimiaceae
- Peumus boldus
- Sarcoplasmic reticulum
ASJC Scopus subject areas
- Drug Discovery
- Analytical Chemistry
- Molecular Medicine
- Complementary and alternative medicine
- Pharmacology
- Pharmaceutical Science
- Organic Chemistry